Unidirectional control of optically induced spin waves

Unidirectional control of optically induced spin waves in a rare-earth iron garnet crystal is demonstrated. We observed the interference of two spin-wave packets with different initial phases generated by circularly polarized light pulses. This interference results in unidirectional propagation if the spin-wave sources are spaced apart at 1/4 of the wavelength of the spin waves and the initial phase difference is set to pi/2. The propagating direction of the spin wave is switched by the polarization helicity of the light pulses. Moreover, in a numerical simulation, applying more than two spin-wave sources with a suitable polarization and spot shape, arbitrary manipulation of the spin wave by the phased array method was replicated

Induced sensorimotor brain plasticity controls pain in phantom limb patients

The cause of pain in a phantom limb after partial or complete deafferentation is an important problem. A popular but increasingly controversial theory is that it results from maladaptive reorganization of the sensorimotor cortex, suggesting that experimental induction of further reorganization should affect the pain, especially if it results in functional restoration. Here we use a brain-machine interface (BMI) based on real-time magnetoencephalography signals to reconstruct affected hand movements with a robotic hand. BMI training induces significant plasticity in the sensorimotor cortex, manifested as improved discriminability of movement information and enhanced prosthetic control. Contrary to our expectation that functional restoration would reduce pain, the BMI training with the phantom hand intensifies the pain. In contrast, BMI training designed to dissociate the prosthetic and phantom hands actually reduces pain. These results reveal a functional relevance between sensorimotor cortical plasticity and pain, and may provide a novel treatment with BMI neurofeedback.This research was conducted under the ‘Development of BMI Technologies for Clinical Application’ of SRPBS by MEXT and AMED. This research was also supported in part by JST PRESTO; JSPS KAKENHI JP24700419, JP26560467, JP22700435, JP26242088, JP26282165, JP15H05710 and JP15H05920; Brain/MINDS and SICP from AMED; ImPACT; Ministry of Health, Labor, and Welfare (18261201); and the Japan Foundation of Aging and Health

Systemic Maternal Inflammation and Neonatal Hyperoxia Induces Remodeling and Left Ventricular Dysfunction in Mice

The impact of the neonatal environment on the development of adult cardiovascular disease is poorly understood. Systemic maternal inflammation is linked to growth retardation, preterm birth, and maturation deficits in the developing fetus. Often preterm or small-for-gestational age infants require medical interventions such as oxygen therapy. The long-term pathological consequences of medical interventions on an immature physiology remain unknown. In the present study, we hypothesized that systemic maternal inflammation and neonatal hyperoxia exposure compromise cardiac structure, resulting in LV dysfunction during adulthood.Pregnant C3H/HeN mice were injected on embryonic day 16 (E16) with LPS (80 µg/kg; i.p.) or saline. Offspring were placed in room air (RA) or 85% O(2) for 14 days and subsequently maintained in RA. Cardiac echocardiography, cardiomyocyte contractility, and molecular analyses were performed. Echocardiography revealed persistent lower left ventricular fractional shortening with greater left ventricular end systolic diameter at 8 weeks in LPS/O(2) than in saline/RA mice. Isolated cardiomyocytes from LPS/O(2) mice had slower rates of contraction and relaxation, and a slower return to baseline length than cardiomyocytes isolated from saline/RA controls. α-/β-MHC ratio was increased and Connexin-43 levels decreased in LPS/O(2) mice at 8 weeks. Nox4 was reduced between day 3 and 14 and capillary density was lower at 8 weeks of life in LPS/O(2) mice.These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health